Search

Supplementary Figures S1-S2; Supplementary Data.

Purpose: Advanced metastatic prostate cancer (PCa) is a fatal disease, with only palliative therapeutic options. Though almost 80% of cases of metastatic PCa present bone metastasis, our current understanding of the molecular mechanisms that govern this metastatic dissemination remains fragmentary. The main objective of the present study was to identify microRNA (miRNA) genes that regulate metastatic PCa.Experimental Design: miRNA expression profiling was done in human prostate cell lines to identify dysregulated miRNA components of advanced PCa. miR-203 expression was assessed in prostate carcinoma cell lines and clinical specimens by real-time PCR and in situ hybridization. To assess the biological significance of miR-203, miR-203 was reexpressed in bone metastatic PCa cell lines followed by in vitro and in vivo functional assays.Results: miR-203 expression is specifically attenuated in bone metastatic PCa suggesting a fundamental antimetastatic role for this miRNA. Reintroduction of miR-203 in bone metastatic PCa cell lines suppresses metastasis via inhibition of several critical steps of the metastatic cascade including epithelial-mesenchymal transition, invasion, and motility. Ectopic miR-203 significantly attenuated the development of metastasis in a bone metastatic model of PCa. Importantly, miR-203 regulates a cohort of pro-metastatic genes including ZEB2, Bmi, survivin, and bone-specific effectors including Runx2, a master regulator of bone metastasis.Conclusions: miR-203 is an “antimetastatic” miRNA in PCa that acts at multiple steps of the PCa metastatic cascade via repression of a cohort of prometastatic targets. miR-203 may be an attractive target for therapeutic intervention in advanced PCa. Clin Cancer Res; 17(16); 5287–98. ©2011 AACR.

Background/Aims We aimed to evaluate the clinical characteristics and long-term prognosis of elderly-onset ulcerative colitis (EOUC) in Korean patients over a 30-year period using a well-established population-based cohort in the Songpa-Kangdong district of Seoul, Korea. Methods Clinical characteristics and prognosis were compared between two groups EOUC, defined as UC diagnosed in individuals aged ≥60 years and non-EOUC (N-EOUC), defined as UC diagnosed in individuals aged 18 to 59 years. Results We identified 99 patients with EOUC (10.3%) and 866 patients with N-EOUC (89.7%) between 1986 and 2015. During the median follow-up of 104.5 months, the overall exposure to medications was comparable between patients with EOUC and N-EOUC (p=0.091 for corticosteroids, p=0.794 for thiopurines, and p=0.095 for anti-tumor necrosis factor agents). The cumulative risks of disease outcomes were also comparable between patients with EOUC and N-EOUC (22.4% vs 30.4% for proximal disease extension [p=0.351], 11.9% vs 18.1% for hospitalization [p=0.240], and 2.3% vs 1.8% for colectomy [p=0.977]) at 10 years after diagnosis. Multivariate Cox regression analysis revealed that corticosteroid use at diagnosis was an independent predictor of proximal disease extension (hazard ratio [HR], 6.216; 95% confidence interval [CI], 1.314 to 28.826) and hospitalization (HR, 11.241; 95% CI, 3.027 to 41.742) in patients with EOUC. Conclusions In this population-based study from Korea, the pattern of medication use seemed comparable between the EOUC and N-EOUC groups. Moreover, patients with EOUC and those with N-EOUC have a similar disease course in terms of proximal disease extension, hospitalization, and colectomy. (Gut Liver 2021;15-751)

ObjectiveNo population-based study has evaluated the natural course of UC over three decades in non-Caucasians. We aimed to assess the long-term natural course of Korean patients with UC in a population-based cohort.DesignThis Korean population-based, Songpa-Kangdong IBD cohort included all patients (n=1013) newly diagnosed with UC during 1986–2015. Disease outcomes and their predictors were evaluated.ResultsDuring the median follow-up of 105 months, the overall use of systemic corticosteroids, thiopurines and antitumour necrosis factor (anti-TNF) agents was 40.8%, 13.9% and 6.5%, respectively. Over time, the cumulative risk of commencing corticosteroids decreased, whereas that of commencing thiopurines and anti-TNF agents increased. During follow-up, 28.7% of 778 patients with proctitis or left-sided colitis at diagnosis experienced proximal disease extension. A total of 28 patients (2.8%) underwent colectomy, demonstrating cumulative risks of colectomy at 1, 5, 10, 20 and 30 years after diagnosis of 1.0%, 1.9%, 2.2%, 5.1% and 6.4%, respectively. Multivariate Cox regression analysis revealed that extensive colitis at diagnosis (HR 8.249, 95% CI 2.394 to 28.430), ever use of corticosteroids (HR 6.437, 95% CI 1.440 to 28.773) and diagnosis in the anti-TNF era (HR 0.224, 95% CI 0.057 to 0.886) were independent predictors of colectomy. The standardised mortality ratio in patients with UC was 0.725 (95% CI 0.508 to 1.004).ConclusionKorean patients with UC may have a better clinical course than Western patients, as indicated by a lower colectomy rate. The overall colectomy rate has continued to decrease over the past three decades.

Background and Aims The long-term outcomes of paediatric-onset inflammatory bowel disease [pIBD] in non-Caucasian populations are unknown. We therefore evaluated and compared the clinical features and long-term outcomes of pIBD with those of adult-onset IBD [aIBD] using a population-based cohort in the Songpa-Kangdong district of Seoul, Korea. Methods Clinical characteristics and prognoses were compared between the two groups: pIBD [defined as Results We identified 131 patients with pIBD (48 ulcerative colitis [UC], 83 Crohn’s disease [CD]) and 1192 patients with aIBD [866 UC, 326 CD] during 1986–2015. Extensive colitis at diagnosis was more prevalent in pUC than in aUC [45.8% vs 22.3%, p < 0.001], and the overall exposure to corticosteroids, thiopurines and anti-tumour necrosis factor agents was higher in pUC than in aUC [p < 0.001]. The cumulative risk of colectomy was higher in pUC than in aUC during a median follow-up of 125.0 and 112.1 months, respectively [8.9% vs 1.8% at 10 years after diagnosis, p = 0.030]. Ileocolonic location and inflammatory behaviour at diagnosis were more common in pCD than in aCD; however, patients with pCD and aCD did not differ regarding treatment or disease course during a median follow-up of 137.2 and 120.9 months, respectively. Conclusion Our study showed clear differences between pIBD and aIBD, especially in UC. pUC presents with more extensive diseases and may have a more severe disease course, as suggested by an earlier time to administering medications and performing colectomy.

Background/Aims The long-term course of Crohn's disease (CD) has never been evaluated in non-Caucasian population-based cohorts. The aim of the present study was to evaluate the longterm prognosis of Korean CD patients in the well-defined population-based Songpa-Kangdong inflammatory bowel disease cohort. Methods Outcomes of disease and their predictors were evaluated for 418 patients diagnosed with CD between 1986 and 2015. Results During a median of 123 months, systemic corticosteroids, thiopurines, and anti-tumor necrosis factor (TNF) agents were administered to 58.6%, 81.3%, and 37.1% of patients, respectively. Over time, the cumulative probability of starting corticosteroids significantly decreased (p=0.001), whereas that of starting thiopurines and anti-TNFs significantly increased (both p

Epstein-Barr virus (EBV) is the cause of infectious mononucleosis, which is characterized by fever, lymphadenopathy, and sore throat. On the other hand, gastrointestinal symptoms of EBV infection like dyspepsia, abdominal pain are non-specific and rarely encountered, which means it is difficult to diagnose gastric involvement of EBV infection without suspicion. The relation between gastric carcinoma and gastric lymphoma associated with EBV infection is well defined, but relations with other EBV-associated gastrointestinal diseases such as gastritis and peptic ulcer disease have rarely been reported. We report a case of benign gastric ulcer with EBV infection confirmed by endoscopic and histological findings.

Background: Maturation failure of autogenous arteriovenous fistula (aAVF) has been increasing after surgical procedures and the salvage percutaneous transluminal angioplasty (sPTA) for immature aAVF has been identified as an effective treatment modality. Objectives: The aim of this study was to identify factors predicting successful aAVF maturation and to determine positive technical aspects of sPTA. Patients and Methods: We retrospectively reviewed medical records and radiological images of 59 patients who had undergone sPTA for non-maturing aAVFs. We analysed images from pre-surgical mapping Doppler ultrasonography, angiography, and angioplasty and follow-up Doppler ultrasonography performed within two weeks after sPTA. We assessed the following factors, for their ability to predict successful aAVF maturation: 1) patient factors (age; sex; co-morbidities; and aAVF age, side and type); 2) vessel factors (cephalic vein diameter and depth, presence of accessory veins, and pre- and postoperative radial artery disease); 3) lesion factors (stenosis number, location and severity); and 4) technical factors (presence of residual stenosis and anatomic success ratio (ASR) on follow-up Doppler ultrasonography). Results: The technical and clinical success rates were both 94.9% (56/59); the mean ASR was 0.84. An ASR of ≥ 0.7 and no significant residual stenosis (< 30%) (both P < 0.001) on two-week follow-up Doppler ultrasonography predicted successful aAVF maturation. Conclusion: For more precise prediction of successful aAVF maturation after sPTA, short-term follow-up Doppler ultrasonography (< 2 weeks) was useful. If the ASR was < 0.7 or if residual stenosis was ≥ 30%, immediate repeat sPTA is recommended.

Purpose: Advanced metastatic prostate cancer (PCa) is a fatal disease, with only palliative therapeutic options. Though almost 80% of cases of metastatic PCa present bone metastasis, our current understanding of the molecular mechanisms that govern this metastatic dissemination remains fragmentary. The main objective of the present study was to identify microRNA (miRNA) genes that regulate metastatic PCa. Experimental Design: miRNA expression profiling was done in human prostate cell lines to identify dysregulated miRNA components of advanced PCa. miR-203 expression was assessed in prostate carcinoma cell lines and clinical specimens by real-time PCR and in situ hybridization. To assess the biological significance of miR-203, miR-203 was reexpressed in bone metastatic PCa cell lines followed by in vitro and in vivo functional assays. Results: miR-203 expression is specifically attenuated in bone metastatic PCa suggesting a fundamental antimetastatic role for this miRNA. Reintroduction of miR-203 in bone metastatic PCa cell lines suppresses metastasis via inhibition of several critical steps of the metastatic cascade including epithelial-mesenchymal transition, invasion, and motility. Ectopic miR-203 significantly attenuated the development of metastasis in a bone metastatic model of PCa. Importantly, miR-203 regulates a cohort of pro-metastatic genes including ZEB2, Bmi, survivin, and bone-specific effectors including Runx2, a master regulator of bone metastasis. Conclusions: miR-203 is an “antimetastatic” miRNA in PCa that acts at multiple steps of the PCa metastatic cascade via repression of a cohort of prometastatic targets. miR-203 may be an attractive target for therapeutic intervention in advanced PCa. Clin Cancer Res; 17(16); 5287–98. ©2011 AACR.

Azathioprine is frequently used for the treatment of inflammatory bowel diseases (IBD) such as Crohn's disease and ulcerative colitis. Lymphomas, squamous cell carcinomas, and undifferentiated pleomorphic sarcomas have been reported among patients receiving azathioprine therapy. Herein, we report a case of pleomorphic liposarcoma of chest wall which occurred in a 44-year-old man with Crohn's disease taking azathioprine. He was diagnosed with Crohn's disease 3 years ago after suffering from abdominal pain and hematochezia for 12 years. He had been taking 50 mg of azathioprine per day for 23 months when he visited the thoracic and cardiovascular surgery clinic due to right chest palpable mass that had rapidly grown during the past 2 months. Excisional biopsy was performed and the mass was diagnosed as pleomorphic liposarcoma. Therefore, he underwent radical excision of the right chest wall mass, which measured 11.0 × 6.5 cm in size. He is scheduled to receive radiation therapy and chemotherapy.

1 and Pathology 2 , National Police Hospital, Seoul, Korea Background/Aims: Incidentally detected focal 18 F-fluorodeoxyglucose (FDG) uptake was compared with colonoscopy. We inves- tigated the characteristics of colon adenomas which were revealed on PET/CT. Then we identified whether additional colonoscopy was necessary in patients with lesions which were revealed on PET/CT but had no matched lesions on colonoscopy. Methods: We retrospectively reviewed 95 patients who underwent colonoscopy within a 6 month interval after they had focal FDG uptake from January 2010 to May 2012 at National Police Hospital in Korea. Also, we analyzed 30 patients who underwent additional colonoscopy within 2 years after they had no matched lesions on primary colonoscopy. Results: PET/CT depicted 54.6% (41/75) of adenomas and adenocarcinomas. The PET visibility of colon adenoma was significantly associated with degree of dysplasia (p=0.027), histologic type (p=0.040), and the size (p=0.038). The positivity rate was increased with higher degree of dysplasia (low-grade dysplasia, 47%; high-grade dysplasia, 78%; adenocarcinoma, 100%) and villous patterns of histologic type (tubular, 46.8%; tubulovillous, 87.5%; villous, 100%). Patients with adenomas larger than 10 mm (87.5%) had higher detection rate compared to those with adenomas smaller than 10 mm (49.0%). Among the 30 patients who underwent additional colonoscopy, only one patient had a 6 mm sized tubular adenoma (low-grade dysplasia). Conclusions: Incidental focal colonic uptake may indicate advanced adenoma or adenocarcinoma. Thus, it justifies performing colonoscopy for identifying the presence of colon neoplasms. However, in case of unmatched lesions between PET/CT and colonoscopy, there was little evidence that additional colonoscopy would yield benefits. (Korean J Gastroenterol 2013;61:319-326)

MiR-145 is downregulated in various cancers including prostate cancer. However, the underlying mechanisms of miR-145 downregulation are not fully understood. Here, we reported that miR-145 was silenced through DNA hypermethylation and p53 mutation status in laser capture microdissected (LCM) prostate cancer and matched adjacent normal tissues. In 22 of 27 (81%) prostate tissues, miR-145 was significantly downregulated in the cancer compared with the normal tissues. Further studies on miR-145 downregulation mechanism showed that miR-145 is methylated at the promoter region in both prostate cancer tissues and 50 different types of cancer cell lines. In seven cancer cell lines with miR-145 hypermethylation, 5-aza-2'-deoxycytidine treatment dramatically induced miR-145 expression. Interestingly, we also found a significant correlation between miR-145 expression and the status of p53 gene in both LCM prostate tissues and 47 cancer cell lines. In 29 cell lines with mutant p53, miR-145 levels were downregulated in 28 lines (97%), whereas in 18 cell lines with wild-type p53 (WT p53), miR-145 levels were downregulated in only 6 lines (33%, P < 0.001). Electrophoretic mobility shift assay showed that p53 binds to the p53 response element upstream of miR-145, but the binding was inhibited by hypermethylation. To further confirm that p53 binding to miR-145 could regulate miR-145 expression, we transfected WT p53 and MUT p53 into PC-3 cells and found that miR-145 is upregulated by WT p53 but not with MUTp53. The apoptotic cells are increased after WT p53 transfection. In summary, this is the first report documenting that downregulation of miR-145 is through DNA methylation and p53 mutation pathways in prostate cancer.

Background: MicroRNAs (miRNAs) are small noncoding RNAs that have important roles in numerous cellular processes. Recent studies have shown aberrant expression of miRNAs in prostate cancer tissues and cell lines. On the basis of miRNA microarray data, we found that miR-145 is significantly downregulated in prostate cancer. Methods and results: We investigated the expression and functional significance of miR-145 in prostate cancer. The expression of miR-145 was low in all the prostate cell lines tested (PC3, LNCaP and DU145) compared with the normal cell line, PWR-1E, and in cancerous regions of human prostate tissue when compared with the matched adjacent normal. Overexpression of miR-145 in PC3-transfected cells resulted in increased apoptosis and an increase in cells in the G2/M phase, as detected by flow cytometry. Investigation of the mechanisms of inactivation of miR-145 through epigenetic pathways revealed significant DNA methylation of the miR-145 promoter region in prostate cancer cell lines. Microarray analyses of miR-145-overexpressing PC3 cells showed upregulation of the pro-apoptotic gene TNFSF10, which was confirmed by real-time PCR and western analysis. Conclusion: One of the genes significantly upregulated by miR-145 overexpression is the proapoptotic gene TNFSF10. Therefore, modulation of miR-145 may be an important therapeutic approach for the management of prostate cancer.

Junction plakoglobin (JUP) is a member of the catenin family that forms complexes with cadherins and these molecules play a role in cell adhesion and motility. Prior studies have demonstrated genetic alterations of the JUP gene to be a risk for diseases. In prostate, expression of JUP has been shown to be down-regulated in the carcinogenesis process and mutations of this gene may play a role in this process. In this study, we hypothesize that polymorphic variants of the JUP gene can be a risk factor for prostate cancer. To test this hypothesis, the genetic distributions of five JUP polymorphisms were analyzed in 131 normal healthy subjects, 132 benign prostatic hyperplasia (BPH), and 177 sporadic prostate cancer samples by sequence-specific PCR and sequencing. The polymorphic sites evaluated were codon 697 (Met to Leu, rs1126821) along with four locations in the promoter region at the following base pairs prior to the ATG start site: -3633 (C to G, rs12450138), -5971 (A to C, 11650969), -9598 (T to C, rs4479305), and -14959 (G to A, rs12937988). Results of these experiments demonstrate that the variants at the -5971 (P Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2773. doi:10.1158/1538-7445.AM2011-2773

Correction to: British Journal of Cancer (2010) 103, 256–264. doi: 10.1038/sj.bjc.6605742 Upon publication of this paper in mid 2010, the authors noted the omission of a grant number in the Acknowledgments section of their paper, which they would now like to correct. They hereby acknowledge the helpof the NIH grant number RO1CA138642.

MiR-145 is down-regulated in various cancers. However, the regulation of miR-145 and its role in the prostate cancer is not known. We analyzed the expression of miR-145 in microdissected prostate cancers and adjacent normal prostate tissues. In 17 of 21 (81%) prostate cancers, the levels of miR-145 (measured by qRT-PCR) were significantly lower than those in the adjacent normal tissues. Down-regulated miR-145 levels correlated with DNA methylation (identified by methylation-specific PCR and sequencing) in the upstream region of miR-145, indicating that methylation may be involved in its regulation. The levels of miR-145 were also measured in 49 cancer cell lines, including 4 prostate cancer, 3 kidney cancer, 11 breast cancer, 23 colorectal cancer and 8 pancreatic cancer cell lines. In cancer cell lines, the down-regulation of miR-145 was also significantly correlated with its methylation. In seven cancer cell lines (3 prostate cancer, 2 kidney cancer and 2 colorectal cancer cell lines) with methylated miR-145, treatment with the demethylation agent, 5-aza-deoxycytidine significantly induced miR-145 expression. We also found a significant correlation between miR-145 expression and the status of the p53 gene in 49 cancer cell lines. In 31 cell lines with a p53 gene mutation, miR-145 levels were low in 30 cell lines (97%) while in 18 cell lines with wild type p53, miR-145 levels were low in only 6 cell lines (33%, p Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2035.

ARHI, an imprinted tumor suppressor gene, is expressed in normal immortalized prostate epithelial cells, but is dramatically down-regulated in prostate cancer cell lines. Here we investigated the mechanisms of ARHI silencing in prostate cancer through microRNA and genistein (a dietary isoflavone from soy) mediated pathways. First, we evaluated ARHI mRNA levels by real time PCR using Q-PCR slice (48 prostate tumor and normal adjacent tissues) and protein levels by immunostaining of prostate tissue array (36 cancer, 8 matched normal adjacent tissue and 4 bone metastases). Both experiments showed down-regulation of ARHI in prostate cancer tissues compared to adjacent normal tissues. To understand the functional significance of ARHI down-regulation with regard to tumorigenesis, ARHI was over-expressed in prostate cancer PC-3 cells by introduction of ARHI plasmid followed by functional studies. Over-expression of ARHI can inhibit cell proliferation, colony formation, invasion and induced caspase-independent apoptosis. Further studies on new mechanism of ARHI down regulation showed a significant inverse relationship between ARHI and miR-221 & 222 which were up-regulated in cancer cell lines. Transfection of miR-221 & 222 inhibitors into PC-3 cells caused a significant induction of ARHI expression. A direct interaction of miR-221 or 222 with a target site on the 3′UTR of ARHI was confirmed by a dual luciferase pMIR-REPORT assay. Finally, we also found that genistein up-regulated ARHI by down regulating miR-221 & 222 in PC-3 cells. In conclusion, ARHI is a tumor suppressor gene down regulated in prostate cancer, and over-expression of ARHI can inhibit cell proliferation, colony formation and invasion. This study demonstrates for the first time that prostate cancer cells have elevated levels of miR-221 & 222 which bind to the 3′UTR of ARHI contributing to its down regulation. Genistein, a potential non-toxic chemopreventive agent restores expression of ARHI and may be an important dietary therapeutic agent for treating prostate cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2090.

MicroRNAs are small noncoding RNAs that play important roles in numerous cellular processes including development, proliferation, and apoptosis. Recent studies have demonstrated aberrant expression of miRNAs in prostate cancer tissues and cell lines. miRNAs microarray data, showed that miR-145 is down-regulated in prostate cancer. Therefore, we investigated the expression and functional significance of miR-145 in prostate cancer. The expression of miR-145 was found to be low in all of the prostate cell lines tested (PC3, LNCaP and DU145). The level of miR-145 expression in adjacent normal regions was found to be significantly higher as compared to the matched cancerous regions. Over expression of miR-145 in PC3 transfected cells resulted in a significant increase in apoptosis and an increase in cells in the G2/M phase, as detected by flow cytometry. Our results also show that methylation of the promoter region of miR-145 in cell lines and carcinoma samples as one of the reasons for its low expression. To identify potential targets for miR-145, we performed microarray analyses in miR-145 over-expressing PC3 cells and observed up regulation of the pro apoptotic gene TNFsf10 which was confirmed by real-time PCR and Western analysis. This is the first report to show that miR-145 acts as a tumor suppressor in prostate cancer through cell cycle arrest and induction of apoptosis. Since a major target for miR-145 is the pro apoptotic TNFsf10 gene, modulation of miR-145 may provide a therapeutic approach for the management of prostate cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2095.

연구배경: 일반적으로 고식적 흉수천자가 어렵다고 판단되는 경우 초음파를 이용한 흉수천자를 영상의학과에 의뢰해 왔다. 영상의학과에 의뢰할 경우 검사를 위해 환자가 직접 이동해야 된다는 불편함과 영상의학과 스케줄에 따라 검사가 지연되거나 비용이 많이 드는 단점이 있다. 이에 저자들은 병실에서 내과 전공의들이 직접 초음파를 이용해서 흉수천자를 시행하는 단계를 포함해서 흉수가 있는 환자에게 접근해보았다. 방 법: 2003년 3월부터 2005년 6월까지 입원한 환자중 흉수가 확인된 환자들을 대상으로 하였고, 흉수의 양이 중등도 이상일 경우에는 고식적 천자를, 흉수의 양이 소량 이거나 소방이 형성된 경우 또는 고식적 천자를 실패 하였을 때에는 초음파를 이용한 천자를 시행하였다. 결 과: 총 89예의 연구대상 가운데 소방의 형성이 없으며 흉수의 양이 대량과 중등도의 양인 79예에서 고식적 흉수천자를 시행하여 74예에서 성공하였다. 고식적 흉수 천자가 실패한 5예와 흉수의 양이 소량인 7예 그리고 소방형성이 있는 3예를 합한 15예에서 초음파를 이용해서 흉수천자를 시행하였고 10예에서 성공하였다(66.7%). 소방이 형성된 3예는 모두 실패하였다. 이 3예를 제외하면 12예 중 10예에서 성공하여 83%의 성공률을 보였다. 2예 (기흉 1예, 혈기흉 1예)에서 합병증이 발생하였다(13.3%). 결 론: 고식적 흉수천자가 실패하였거나 흉수의 양이 소량인 경우, 병실에서 내과 전공의가 초음파를 이용하여 흉수천자를 시행하는 것이 비교적 효과적이고 안전할 것으로 사료된다. 그러나 소방이 형성된 경우에는 영상의학과에 먼저 의뢰하는 것이 좋을 것으로 판단된다.